This document summarizes a thesis submitted by Eliot Mar examining whether the amount of naturally occurring UV radiation affects stress fracture rates in female athletes via changes in vitamin D production. The document provides background on vitamin D production and role in bone health, defines stress fractures and the female athlete triad, and reviews studies examining the relationship between UV exposure, vitamin D levels, and stress fracture rates in female athletes and military recruits. The thesis examines whether female athletes in areas with lower annual UV radiation are at higher risk of stress fractures compared to those in areas with higher UV radiation.

1. Does the amount of naturally occurring UV radiation affect stress fracture rates in female
athletes via changes in vitamin D production?
by
Eliot Mar
A thesis submitted to the General Science Department of Seattle University in Partial
Fulfillment of the Requirements for the Degree
BACHELOR OF SCIENCE
Seattle, WA
2014

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Abstract:
Vitamin D deficiency, also known as hypovitaminosis D, is a common health
affliction of a large part of the American population. Vitamin D is produced naturally by
the body in response to sunlight via photolytic reaction in the skin and regulates calcium
levels in the body as well as bone health and density. Women are biologically more at
risk than men to be vitamin D deficient and are at greater risk for bone related injuries.
Studies have shown difference in bone health between genders, as well as the production
of vitamin D via UV radiation. The effect, however, of UV radiation on female athletes in
high physical intensity environments involving risk of bone injury have not been as
thoroughly tested. Given that vitamin D controls bone health, female athletes who are in
environments high of risk of bone related injury such as stress fracture, amounts of UV
radiation should affect the percentage occurrence of injury.
Introduction:
Vitamin D deficiency is a major health issue for people in the United States. A
study by Leidig-Bruckner et al. in 2011 suggested that as few as 20% of ambulatory
(mobile) patients 14-60 years old had high enough vitamin D levels to prevent vitamin D
related bone diseases and bone injury.i A previous study of a larger survey population
from Karl McClung suggested that hypovitaminosis D, could affect up to 40% of men
and 51% of women with levels being “significantly higher for women and minorities as
compared to white men.”ii The primary concern with hypovitaminosis D is in vitamin D’s

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regulatory role in parathyroid hormone (PTH) and calcium levels in bone tissue. Vitamin
D is directly related to the production of PTH in the parathyroid gland. This hormone is
responsible for controlling the levels of calcium in bone tissue which, in turn, can be used
as indicators of bone density and strength. For this reason, the most common type of bone
related injury occurs in the form of stress fractures, or injury brought about by “recurring
excessive strain caused by repetitive micro-trauma to bone at a rate greater than bone
repair.”iii It is an overuse injury, where “the muscles of the affected area become
fatigued,” and the impact or stress is then “transferred to the bone, resulting in a small
crack…”iv The role of sunlight as it pertains to stress fractures is therefore paramount as
it directly relates to the amount of vitamin D produced. The more vitamin D in the body,
the greater the rate of bone repair in relation to the rate of the micro-traumas caused by
the impact and excessive strain that can lead to stress fractures.
According to Rosenbloom, "40% of athletes report a stress fracture at some time
in their career.”4 Bone density loss, the cause of the stress fracturing, is a part of what is
known as the “female athlete triad.” This triad is composed of three deficiencies resultant
of rigorous physical activity: Menstrual dysfunction, (defined as oligomenorrhea or less
than 9 periods per year), which causes suppression of hormone production and bone loss;
low energy availability, and overall loss of bone density. Though being afflicted with the
female athlete triad is not prevalent among female athletes, almost one in four female
athletes suffer from at least one component of the triad due to their training regiment
leading to an according loss in bone density. This bone loss related to the female athlete
triad has been thoroughly studied and the long term effects have been recorded to
include, amenorrhea, infertility, increased fracture risk, bone disease such as osteoporosis

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and osteoarthritis and even diminished capacity for arterial vasodilation leading to
cardiovascular disease and disorders.4
Much of the research regarding stress fractures and hypovitaminosis D has
focused on comparison of dietary and supplemental vitamin D intake. As popular and as
highly contested as daily recommended healthy amounts of vitamin D are, comparison of
stress fracture rate and relative UV radiation exposure has not been as extensively
studied. Given the prevalence of vitamin D deficiency and that women are more likely to
experience hypovitaminosis D, the most at risk populations for stress fracture are those of
women in environments involving high volumes of strenuous, consistent physical activity
and lacking stimulation of vitamin D production. Women in the armed forces and female
athletes are therefore included as high-risk groups. Due to the aforementioned factors,
female athletes in areas of low annual UV radiation and exposure are at a higher risk than
those athletes in areas of high annual UV radiation and exposure for stress fracture.
Background:
Vitamin D is responsible for controlling the feedback loop between parathyroid
hormone, (PTH), and calcitonin hormone
levels in blood plasma. Both hormones
regulate absorption of calcium by the
intestines and osteoclast activity in breaking
down bone material to release calcium from
the bone matrix. Production of vitamin D
occurs naturally in the body in response to
Figure 1: UV radiation to vitamin D
mechanism6

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skin’s exposure to UV radiation from sunlight. This photolytic reaction converting
ultraviolet radiation into vitamin D involves conversion of 7-dehydrocholesterol into two
types of vitamin D commonly found in the blood: 25-hydroxyvitamin D, (25(OH)D), and
1,25-dihydroxyvitamin D, (1,25(OH)2D)).v Mechanistically, the interaction of vitamin D
binding to the vitamin D receptors, (VDR), in the body acts to keep calcium absorption
rates of the body in homeostasis. When more vitamin D is bound to VDR, the intestines
absorb more calcium and osteoclast activity is suppressed leading to maintained or
increased bone density and health. Less vitamin D bound to VDR, as is the case when
hypovitaminosis D occurs, leads to an increase in PTH secretion and osteoclast
breakdown of bone resulting in a decrease in bone density. More specifically, sunlight
causes activation of 7-dehydroxycholesterol which is converted to cholecalciferol steroid
hormone or vitamin D3. Cholecalciferol is then converted in the liver to 25-
Dihydroxyvitamin D3 where it is further processed by the kidneys into 1.25-
Dihydroxyvitamin D3 or, as it has been referred to earlier in this paper, (1,25(OH)2D)).vi
From the kidneys, PTH acts on feedback from the body in response to calcium blood
plasma levels to regulate release of (1,25(OH)2D)) to bind to VDR receptors in the body
and VDR receptors in the intestines. Exposure to sunlight leads to production of the
steroid hormone cholecalciferol and production of (1,25(OH)2D)). High levels of
(1,25(OH)2D)) binding to VDR causes an increase in calcium absorption in the small
intestine, an increase in reabsorption of calcium in the kidneys and suppression of
osteoclast activity leading to an increase or maintenance in bone density.
Though the causality of hypovitaminosis is well known, a current consensus on
minimum daily-recommended amounts of vitamin D for a person has yet to be agreed

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upon. Currently, blood concentration levels greater than or equal to 75 nmol/L for blood
plasma concentration are the most widely agreed upon but still does not address the
problem of the affect metabolic rates. Studies involving participants in environments of
high physical stress with a range of low to high concentrations of UV radiation have been
done to compare the hypothesized adverse affects to bone health in areas of low UV
radiation may have. UV radiation is most commonly measured by the intensity of
sunlight per year as is given by the UV index provided by organizations such as NOAA
or the national weather service.vii
Vitamin D deficiency, (hypovitaminosis D), is “unique in that it may be obtained
from the diet or synthesized in the skin in the presence of ultraviolet B (UVB) light (290-
315 nm).”viii Hypovitaminosis D can be caused by a plethora of different contributing
factors aside from lack of sunlight though. Besides its effect on PTH regulation, vitamin
D is responsible for “calcium handling and transport, phosphate metabolism, cytoskeletal
protein expression, and the activation of mitogen activate protein kinase signaling
pathways in skeletal muscle.”2 As was previously mentioned by Rosenblom, stress
fractures result from muscular fatigue leading to displacement of force upon the bones of
the body.4 Hypovitaminosis can also be caused by moderate to severe lack of dietary
consumption of vitamin D. As in the case in female athletes with one or more aspects of
the female athlete triad, aesthetic concern about appearing “thin” and the caloric and
energy demands of intense training cause an imbalance in nutritional intake less than
what is necessary for the body to healthily function.

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Female Athlete Triad:
“Low energy availability, menstrual disturbances and low bone mineral density,”
is known as the “female athlete triad.”ix The triad is comprised of three parts being
amenorrhea, osteoporosis or bone disease, and low energy availability.4 A primary cause
of any of the three components of the female athlete triad includes a high demand and
physical taxation on the body coupled with an aesthetic desire for thinness that may limit
energy availability through dietary deficiency. Components of the female athlete triad can
be brought about by hypovitaminosis D. Most notably, menstrual disturbances and low
bone mineral density can be symptoms brought about by vitamin D deficiencies. An
irregular menstrual cycle, (oligorrhoea), or not having menses for 3 month periods,
(amenorrhea), as a part of the female athlete triad causes hormonal imbalances that
disrupt the activity of hormones such as PTH and calcitonin that maintain bone density
and Calcium blood plasma levels.8 It is estimated that, although percentages of female
athletes suffering from all three aspects of the “female athlete triad are low, almost 20-
25% of female athletes have at least 1 component of the triad.”4
Despite the variability of factors affecting cutaneous or skin exposure to UV
radiation for female athletes across all sports, observation of vitamin D levels in athletes
as a contributing factor to stress fracturing has not been widely tested. The general
consensus for treating amenorrhea brought about by hypovitaminosis D and calcium
deficiency has been through dietary supplementation in calcium and vitamin D.4 Studies
have shown a trend in female athletes over time for greater incidence of stress fractures to
occur. In an analysis of incidences of stress fracture at the collegiate level, athletes in
running sports such as track or distance running experienced up to a 21% stress fracture

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rate among female athletes within a one year period. Though the difference in
occurrences of stress fractures by gender was not statistically significant for most of the
studies done by female and male populations in athletics and the military, the parts of the
studies that were conducted over a 10 year minimum period did show large differences
between genders with female athletes reporting cases of stress fractures in lower limb
bones at higher frequency than males. This data showed averages of ~6.5% in males and
~9.2% in females.3
Affects of the female athlete triad on susceptibility for stress fracture may be
higher than reported due to the fact that many sports are not as lower body intensive. The
most common injuries, for biomechanical reasons relating to hip angle and displacement
of force and weight on the lower limb bones in females, are at the tibia, metatarsals,
femur, and calcaneus, bones.3 Women are at a higher risk of lower body injury due to
having a wider pelvis which “alters the angular tilt on the hips and knees, increasing the
stress” on the lower body bones.3 The difference in the anatomy of the female pelvis
leads to an increase in distribution of weight or “loading strain” on the lower limbs and
therefore an increase in occurrence of stress fractures among female athletes as compared
to their male counterparts undergoing similar levels of activity.3 Statistically the
percentages of female athletes who have calcium deficiencies and/or hypovitaminosis D
support that all female athletes are at least at risk for stress fracture and not just female
runners.
Sunlight deprivation:

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Vitamin D deficiency on the basis of lack of sunlight can be determined by
controlling the variables of race, gender, and dietary supplementation. A study by
Iuliano-Burns et al. suggested that insufficient exposure to sunlight can cause
hypovitaminosis D.5 In the study, Antarctic expeditioners were in environments of both
intense and predictable sunlight seasonal patterns. The climate of the Antarctic was ideal
to measure prolonged exposure to sunlight against prolonged periods of no or low
sunlight, from approximately March to September, when “negligible” UV sunlight is
available. Their hypothesis was that, as the diets of the Antarctic expeditioners5 were
simultaneously and randomly (double blind test) withheld vitamin D dietary
supplementation, a consistent (monthly) doses of supplemental vitamin D would result in
a decrease in PTH activity and conserve bone density. Baseline averages of 1,600 IU, 800
IU, and 100 IU per day were used and measurements of bone density were taken at the
proximal femur and lower spine as the lower body is the most common site of fracture
associated with hypovitaminosis D.v The major problem encountered by this study was in
the inability to create a true a group of expeditioners who did not receive any
supplemental vitamin D in combination with lack of UV radiation as a photolytic source
of vitamin D. This would have been unethical practice in knowingly subjecting a test
group to conditions with heightened risk of stress fracture. Over the six month duration of
the study, the respective daily values of supplemental vitamin D were administered at
monthly, bi-monthly, and one single large dose to study participants.5 This method of
testing was administered to three different test groups having the administration of the
doses of vitamin D as the variable changed and recorded. The results of this study found

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that the single large initial dose of vitamin D had a greater effect than the monthly and bi-
monthly supplementations.
Though the study’s focus was on the effect of dietary supplementation of vitamin
D on combating vitamin D deficiency, UV radiation was observed as a means of inducing
or controlling hypovitaminosis D. Through UV deprivation, all participants in the study
experienced hypovitaminosis D. Lack of UV radiation as a source of sufficient vitamin D
supports the importance of UV radiation as a major contributor to production of vitamin
D in the body and maintenance of homeostatic bone density.
In a related study on UV indexing by Scott Montain et al., geographic effect on
bone health was observed in order to determine the degree to which hypovitaminosis
occurred in areas of low UV index as opposed to areas of high UV index. Quantitative
data of the study was collected by dividing up the “48 contiguous states and Alaska into
144 cells” and recording the average UV radiation indexes for the 200 major cities within
each cell.6 Female populations in the military going through basic combat training (BCT)
and female collegiate athletes were observed.6 This study hypothesized that “darker
complexions” would make UV absorption more difficult and thereby limit the amount of
vitamin D producible with comparable sunlight exposure for people with lighter skin
pigmentations. Comparatively, female U.S. navy recruits with 25-hydroxyvitamin D
levels less than 20ng/mL were found to have a higher occurrence of stress fracture than
recruits with 25-hydroxyvitamin D levels greater than 40 ng/mL. As the study progressed
to compare the relative stress fracture rates based on the pigmentation of the participant’s
skin, it was found that white females with high 25-hydroxyvitamin D plasma levels had a
lower risk of stress fracture than those with low 25-hydroxyvitamin D plasma levels. The

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same paradigm was not observed in other ethnicities. African, Asian, Hispanic, and
Native American women did not express the expected result of consistently lower rates of
stress fracture than white females due to their skin pigmentation acting as an obstacle to
UV radiation absorbtion.6
The postulation by this study that UV radiation levels, as affected by skin
complexion, do not have an effect on bone density or stress fracture rate was supported
by the lack of statistically relevant difference between females in the military with darker
skin compared to white females. Among the 2% of surveyed members of the military
who report stress fractures, women in general were shown to have between 2 and 10
times higher rates of fracture than men. The data of the study, however, showed that
“black men and women have had lower incidences of stress fractures than white men and
women performing the same military training.”6 Statistically, “10% and 5% of white and
black females developed stress fractures, respectively, during nine weeks of Navy basic
training,” and “3% and 1.4% of white and black trainees, respectively, were removed
from [basic combat training] to recover from stress fractures developed during training.”6
Both these findings suggest a difference in rate of stress fracture as a function of ethnicity
and, accordingly, UV radiation’s impact on vitamin D production. It was shown that
recruits coming from areas of low annual average sunlight HOR, (homes of residence),
did not exhibit a higher predisposition to experiencing stress fractures. Per 1000 recruits,
the stress fractures for “low, moderate and high UV index regions” were 26, 31.3 and
31.1 respectively.6 It was also shown that “non-blacks were more likely than blacks to
develop lower limb fractures…”6 UV radiation’s role in vitamin D production is
diminished as available sunlight for absorption decreases. Skin pigmentation limits the

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amount of UV radiation able to be taken in by the body and used for natural production
of vitamin D.3 Though it was hypothesized that people with darker completions would be
more likely to experience stress fracturing, the results refuted conclusive evidence
supporting darker skin pigmentation as an obstacle to UV radiation absorption.
The conclusion of the study was that low UV levels did not contribute
significantly to an increase in stress fracture rate. Instead, the study suggested
“individuals entering military service from areas with a low annualized UV index were
actually less likely to suffer a stress fracture than those entering from a high UV intensity
area.”6 Though this finding may seem to refute the hypothesis that there is a direct
correlation between higher levels of UV radiation in a given area and bone density and
stress fracture rate, it actually acts to support the theory. The surveyed subjects were all
tested at locations on military and navy bases. Using this fact as a control, these fixed
locations were themselves located in their own geographic UV index cell. The major
army and navy bases in the United States fall mostly within what the study defined as low
or moderate UV index regions. Individuals coming from low UV index regions may have
been able to more efficiently use vitamin D than individuals with previous exposure to
high UV index regions.
Vitamin D and Collegiate Athletes:
A study by Tanya M. Halliday et al. examined NCAA DI athletes and observed
the relationship between 25-Dihydroxyvitamin D blood plasma concentration and overall
vitamin D dietary intake, UV radiation exposure, and body compsition. It also
secondarily “evaluated whether 25-Dihydroxyvitamin D concentration is linked to bone

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density, development of overuse or inflammatory injuries, and/or incidence of frequent
illness”9 Individuals tested were male and female NCAA DI athletes over the age of 18
from the University of Wyoming. All athletes started without preexisting injuries and
were then split into indoor or outdoor athletes. Athletes who participated in football,
soccer, cross-country or track and field were considered outdoor athletes.9 Athletes in
wrestling, swimming, and basketball were considered outdoor athletes.9 Bone density and
PTH blood plasma concentrations were taken at seasonal intervals and any bone related
injuries that occurred over the course of the study were recorded.6 The results of the
survey, were as follows: overall, 9.8% of the athletes in the fall were found to be vitamin
D deficient. In the winter, 60.6 % of athletes were found to be vitamin D deficient. In the
spring, 4% of athletes were found to be vitamin D deficient. When comparing outdoor to
indoor athletes, 53.1% vs 31.9% of fall athletes, 31.9% to 10.2% of winter athletes, and
44.6% to 33.1% of spring athletes showed higher vitamin D blood plasma levels.9 The
report noted that, though a difference in UV radiation exposure contributed to higher
levels of vitamin D in blood plasma, no difference in concentration of 25-
Dihydroxyvitamin D was found between genders. The study suggested “that athletes who
[practiced] indoors [were] at risk for vitamin D insufficiency and deficiency…”ix and the
athletes experienced an expected decrease in 25-Dihydroxyvitamin D blood plasma
concentration levels in the winter as compared to the spring and fall when sunlight is
seasonally more intense and consistently available. It was also found that there was a
“lack of a relation between vitamin D status” and consumption of vitamin D via dietary
supplementation.

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Dietary supplementation as a primary source of vitamin D though was shown not
sufficient or as effective as that of UV radiation. 25-Dihydroxyvitamin D blood plasma
levels and PTH blood plasma levels are known to regulate the release or suppression of
osteoclast cells in the body causing an increase or decrease in bone density. Halliday et
al.’s focus upon the impact of sources of vitamin D on 25-Dihydroxyvitamin D
concentration in the body depending on relative seasonal sunlight, (UV index), and
dietary supplementation strongly support a correlation between receiving enough natural
UV radiation over a prolonged period of time and a lowered risk for stress fracturing. The
target test group included college female athletes ages 18 and up who fit the description
of people at high risk for stress fracture based on their consistent and sustained intense
physical activity. The study found that limiting the availability and consumption of
vitamin D rich foods, dietary supplementation of vitamin D made a negligible impact on
the test group. The observable changes then, were attributed to the changes in the
geography or climate the athlete trained in. Based on the change in environment, whether
it was between indoor and outdoor (less sunlight to more sunlight exposure) or what
season the athlete’s participated in their respective sports, a direct correlation between
more UV radiation and more 25-Dihydroxyvitamin D concentration was supported. As it
has already been established that 25-Dihydroxyvitamin D’s interaction with VDR also
has a direct correlation with stress fracture rate via PTH and bone density regulation, it
follows that the study also supports a relationship between UV radiation and stress
fracture rate.

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Summarizing factors of stress fracture:
Physical activity itself “has been associated with improvements in bone health, as
such, physical training regimens may provide an important opportunity for athletes or
populations engaged in physically demanding activities to maximize bone strength such
that future bone injuries may be avoided.”x A study by James McClung explained the
primary factors affecting stress fracture risk, were age, vitamin D concentration in blood
plasma, gender, whether or not a person smokes, amenorrhea, and polymorphisms in
VDR.10 With respect to gender, he found that 21% of females experienced stress
fracturing compared to just 5% in men among the general military population.10 A study
involving comparison of twins suggested that VDR polymorphisms or genotypic
differences play a role in determining risk of stress fracture. The study suggested that “up
to 75% of the variation in peak bone mass” could be due to VDR variation and “up to
80% of the variability in [bone mass density] may be explained by genetic factors.”10
This would suggest that the other factors such as sunlight exposure and dietary
consumption of vitamin D may only show measurable difference in individuals where a
genetic predisposition to poor uptake or inefficient activity of VDR and 25-
Dihydroxyvitamin D has not already taken precedence as the primary cause of
hypovitaminosis D.
Treatment strategies:
Treatment of hypovitaminosis D and treatment of stress fractures involve both pre
and post habilitation solutions. Preventative measures for vitamin D deficiency,

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excluding VDR polymorphisms as the cause, involve a diet where vitamin D rich foods
are consumed in secondary support of exposure to UV radiation in order to stimulate
natural vitamin D production in the body. Preventative exercises such as stretching and
lighter intensity workouts, also known as prehabilitation, do not have as well defined
parameters. Physical activity is known to improve bone health to a degree, yet stress
fracturing itself is caused by an excess of physical activity in the form of overuse and
overtraining. Because of this, finding a balance between rest to avoid muscular fatigue
and training is the best solution to avoid stress fracturing. Female athletes already
experiencing hypovitaminosis D can be treated through similar approaches to
prehabilitation measures with increases in 25-Dihydroxyvitamin D supplementation or, in
the case of the amenorrhetic component of the female athlete triad, hormone therapy, or a
prolonged break from or diminished intensity of workouts. This can restore homeostatic
regulation of PTH and calcitonin in the body, making better use of 25-Dihydroxyvitamin
D and dampening the effects of low vitamin D blood plasma levels. Though these
measures are not as efficient or preferable to naturally produced vitamin D, they do help
to lessen the risk of stress fracture and do help promote bone health. Rehabilitation for
stress fractures mainly involves time as the cause of fracture stems from bone trauma
happening at a greater rate then the body is able to rebuild bone.
Conclusions:
Female athletes who train in areas of high annual UV radiation have the
advantage of a readily available and constant source of vitamin D production over female
athletes in areas of low annual UV radiation. As suggested by Scott J Montain et al,

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preconditioning to UV radiation may play a larger role in ability to efficiently absorb
vitamin D and therefore UV radiation in itself may not be directly responsible for bone
health or stress fracture rate.6 As was previously mentioned in the study by McClung on
vitamin D and stress fracture, the contribution of vitamin D receptor gene polymorphisms
also suggest that UV radiation’s varied affect on bone density may be due more to
genetic factors than other mitigating variables.10 Both of these studies, though strongly
supported, also concluded that many environmental factors had to be ignored in order to
create observable control groups. Scientific evidence backing a correlation between UV
radiation and stress fracture rate has been difficult to prove or test given the range of
factors contributing to vitamin D production, activity between vitamin D and VDR and
PTH, and bone density in general. Despite the lack of clinical evidence to support a
connection between UV radiation and stress fracturing, there is strong biochemical
mechanistic evidence backing the claim that female athletes in areas of high annual UV
radiation are at lesser risk for stress fracturing than female athletes in areas of low annual
UV radiation.

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Lorenz A, Raue F, Frank-Raue K. Osteoporos. Int. 22, 231–240.
ii Barker, Tyler; Schneider, Erik D;
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iii Wentz, Laurel; Liu, Pei-yang; Hay, Emily; Ilich, Jasminka Z 176, 420–431.
iv Rosenblom, Christine. Nutrition Today. 48, 81-87
v Iuliano-Burns, S; Ayton,J; Hillam, S; Jones,G; King, K; Macleod, S; Seeman, E. Osterooros. Int. 23,
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vi Borradale, David; Kimlin, Michael. Nutr. Res. Rev. 22, 118–36.
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Musculoskelet.Disord. 14, 135.
viii Halliday, Tanya M; Peterson,Nikki J; Thomas, Joi J; Kleppinger, Kent; Hollis, Bruce W; Larson-Meyer,
D Enette. Med. Sci. SportsExerc. 43, 335–43.
ix Ducher, Gaele; Turner, Anne I; Kukuljan, Sonja; Pantano,Kathleen J; Carlson, Jennifer L; Williams,
Nancy I; Souza, Mary Jane De. 41, 587–608.
x McClung, James P; Karl, J Philip. Nutr. Rev. 68, 365–9.